The disabling or lethal syndromes of refractory hypertension, Raynaud's syndrome, myocardial infarction and cardiac arrhythmias may be associated with high circulating catecholamines and/or vasoconstrictor phenomena. Concentrations of norepinephrine in plasma are frequently elevated in patients with myocardial infarction and arrhythmias and in refractory hypertensives treated with vasodilator drugs, but have not been well studied in Raynaud's syndrome. Clonidine, while having some limitation in usefulness clinically because of side effects, is a powerful tool in down-regulating or suppressing the sympathetic nervous system. We propose first to characterize suppression of the sympathetic nervous system by clonidine, using circulating norepinephrine levels, blood pressure, and heart rate as indices of effect. Dose-response and chronology thereof will be studied in two types of patients: 1) those with essential hypertension who generally have normal or near normal circulating norepinephrine levels; and 2) vasodilator and beta-blocker drug treated severely hypertensive subjects who have high levels of circulating norepinephrine levels. We propose to then test the hypothesis that suppression of the sympathetic nervous system, using clonidine as a tool, will influence symptoms and/or the course of the disease in several cardiovascular syndromes including those listed above.